Heart is not like a rigid structure built with bricks . . . . so , its too architectural mindset to describe cardiac chambers to be made up of walls. Rather , Its a four chambered muscle mass moulded together in a complex 3D interface with distinct surfaces rather than walls. It’s also important to realise, since the heart is positioned (rather hanging )delicately in the middle mediastinum resting on the diaphragm , its subjected to one more dynamism due to respiratory motion blurring the definition of surfaces as well. (Vertical vs Horizontal)

Posterior surface is now referred to as infero-posterior

The posterior aspect of heart contains essentially the venous channels and the atrium (LA in particular)pulmonary veins and coronary sinus. This happens right from 8 week heart open stage when venous end of lower straight heart tube folds up and posteriorly .

It should be recalled only a small portion of lower aspect of posterior wall is alloted to left ventrilce.Instead the Infero diaphragmatic surface is formed by two-thirds the LV and one-third Right ventricle.

Image courtesy : From the great Netter

Nomenclature issue

The term posterior wall is now abandoned in most Echocardiography texts its replaced by inferior .The implication is more for Electrophysiologists with reference to accessory pathway localization

What is true posterior wall MI ?

As discussed before ,posterior surface of heart is different from posterior aspect of left and and right ventricle.

What does leads V7 V8 V9 record ?

It actually records electrical signals arising from posterior aspect of heart. Left atrium, pulmonary vein along with insulatory effect of lungs dampens the potential . This makes the sensitivity of ST elevation in posterior MI is low.

Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.

Real life experience now suggest, a bothering number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in every seizure disorder. As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)

There are important diseases that restricts entry of blood into right heart chambers. They can occur either in an acute (Tamponade) or in chronic fashion like constrictive pericarditis and restrictive cardiomyopathy.These entities show distinctive impact on JVP and systemic pulse.

The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the arterial counter part of Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.

* Pulsus paradoxus is a term originally used by Kussmaul when he noted heart sounds were retained while pulse dissappeared in patients with cardiac tamponade .Later we realised the loss of pulse was linked to inspiratory cycle of respiration. To make this sign objective sphygmomanometery criteria was formulated which measured the difference between inspiratory and expiratory korotkoff’s sounds .

Coming up next

Why Kussmaul sign is often absent in Tamponade while its arterial counterpart pulsus paradoxus may still be conspicuous ?

We know aortic regurgitation causes a deluge of hugely popular peripheral signs of aortic run off , which are taught right from 2nd year medical school.

When the aorta leaks it reflects in the entire vascular tree .How is that a leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?

Is the blood in the finger trying to follow the regurgitant jet that go back into left ventricle ? Does the to and fro murmur of Duroziez over the femoral artery imply there is reversal of blood flow in femoral artery ?

Things are little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is dramatically low in chronic severe AR by a reflex phenomenon , as cardiac out put is increased and vascular tree adopt to it. So, with each beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of blood runs off , as if it goes in a free way making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR are due to the peripheral mechanisms rather than primary event of aortic run off into left ventricle.

Why carotid pulse does not show the collapsible nature of pulse in AR ?

If aortic leak into LV is the dominant mechanism , carotid artery should obviously manifest a collapse ,but it doesn’t ,as carotid has no direct continuity with the peripheral low resistance circuit

What is the hemo-dynamic correlates of descending aortic flow reversal in severe AR ?

The central vascular tree manifest some reversal till the regurgitant velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise it is only the wave form that get reversed not the actual blood stream.( The momentum gained in systole continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are absent in acute AR ?

Acute AR even if it’s significant does not cause a collapsing pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.

Summary

Answering the title question ,the mechanism of Aortic run off in AR is both central and peripheral. However clinical signs are largely due to high cardiac out put and the resultant adaptive response of the vascular tree due to low systemic vascular resistance triggered by reflex dilatation of small arteriolesof the peripheral vascular bed.

When a patient comes with angina at rest , it could mean two things .Either a STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the character of chest pain alone ?

Very tough task isn’t ? But there are some definite clues .

Infarct pain

Is mostly sudden .

Likely to be crescendo , lasts more than 20-30 minutes .

Fails to get relived by rest or even Nitrites.

Sweating due to sympathetic activation is more pronounced.

Unstable angina

Is rarely sudden .Often has a pro-drome.

UA is mostly precipitated by an increased demand situation or a stress.

It has a typical waxing and waning pattern . Rarely assume a true crescendo character as myocytes does not necrose (Just threaten to die !)

The chest pain radiation to shoulder is less conspicuous , instead it tends to reach the jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is due to subtotal occlusion and endocardial ischemia , while STEMI is sudden total occlusion and the resultant transmural ischemia . In STEMI epicardial surface is always involved (Which lifts the ST segment in ECG .).We know epicardium is same as visceral layer of pericardium which is well innervated .Hence pain of STEMI acquires more of somatic character than a predominately visceral type pain that occurs with UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue to differentiate the chest pain of STEMI and NSTEMI .A significant overlap can occur in real coronary care scenario . We know chest pain that occurs in both pre and post infarct phase is considered as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating them may even be termed as futile.

Still,clinical cardiology can be made fascinating by indulging in such exercise !

This query often evokes confusion among fellows and General physicians .

The answer is simple .Yes , you can.(With few conditions)

Thrombolysis or PCI is done with reference to the presence or absence of ST elevation and chest pain.

If there is ongoing chest pain and significant new onset ST elevation thrombolysis or PCI is indicated whether there is associated q waves or not.

Clinical situations

Ischemic q waves: Q wave can occur with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them regenerate this R within few days after STEMI , indicating the q waves can be ischemic in origin)

Reinfarction : Patients with old MI can develop fresh ST elevation in q leads due to tachycardia and dyskinetic infarct segment .This group of patients should be carefully evaluated before labeling them as re-infarction

* q RBBB in early hours of anterior STEMI is fairly common which may revert later. qRBBB is not a contraindication for re-perfusion .

Final message

Presence of q waves does not imply one should not entertain thrombolysis or PCI .The decision to reperfuse , rather goes with presence of chest pain , ST elevation and of course within the acceptable time window!

The right ventricle is considered as a docilecardiac chamber with passive filling and emptying properties .

This belief was reinforced when Fontan in early 1970s suggested a principle in the management of cyanotic heart disease when the right side of the heart is underdeveloped. He proved RV can be by-passed safely , with great veins (IVC/SVC) by themselves take care of filling the pulmonary circulation without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading concept. In clinical cardiology practice ,sudden or non sudden RV deaths happen every day in the form of . . .

RV Infarction

Acute RV dysfunction in massive pulmonary embolism

COPD with RV dysfunction

Most cases dilated cardiomypathy the terminal event is due to RV failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and hemodynamics . We are getting more insights from modern blood pool imaging by MRI , about how the RV handles the blood volume .

I stumbled upon this excellent work by Alexandru G.Fredriksson published in APS (American physiology society ) This MRI study have documented RV fucntion in a dramatic fashion.

We know RV has a unique shape triangular ( partially pyramidal ) . It can be inferred the RV cavity is formed by fusion of many eccentric spacial planes. We have always believed RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.

It is curious to know RV inflow is connected to the outflow by an invisible physiologic Bridge . About 44% of blood traverse the RV in this fashion.

Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical function of RVOT could be most vital. If it fails to handle the first increment which comes directly from RV inflow, stasis is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

We need to analyse why RV dilates in some but goes for hypertrophyin others when confronted with pressure overload (VPS vs PAH)

RV apical clot in restrictive cardiomyopathy is a direct consequence of stasis of blood in RV apical zone .

RVOT pacing may have a hemodynamic advantage over RV apical pacing . However , for anatomical reasons RV apical pacing is far safer than RVOT pacing where the lead is subjected to constant life long strain due to this busy RV inflow to outflow express high way !

Final message

Traditionally we have labeled RV as a passive venous chamber .It is clearly a misnomer.It has to handle both the venous and pumping function beat to beat with precision without back log .Obviously , RV has to think and work more than it’s big brother !

Reference

I wonder , if there is any other site other than APS . . . to find crucial answers in cardiac physiology !

After thought

There is huge gap between physiologists who work in research labs and the physicians at bed side .

I appeal all young cardiologists to visit APS once in a while ,between your busy cath lab schedule and help narrow this gap.

Without understanding the physiology properly how are we going to intervene the pathology ?